Mitochondrial dysfunction and mitophagy in Parkinson's: from familial to sporadic disease.
Identifieur interne : 001A90 ( Ncbi/Merge ); précédent : 001A89; suivant : 001A91Mitochondrial dysfunction and mitophagy in Parkinson's: from familial to sporadic disease.
Auteurs : Brent J. Ryan [Royaume-Uni] ; Selim Hoek [Royaume-Uni] ; Edward A. Fon [Canada] ; Richard Wade-Martins [Royaume-Uni]Source :
- Trends in biochemical sciences [ 0968-0004 ] ; 2015.
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : alpha-Synuclein.
- metabolism : Mitochondria, Parkinson Disease.
- pathology : Mitochondria, Parkinson Disease.
- Animals, Humans.
Abstract
Parkinson's disease (PD) is a progressive neurodegenerative disorder characterised by the preferential loss of dopaminergic neurons in the substantia nigra. Mitochondrial dysfunction is increasingly appreciated as a key determinant of dopaminergic neuronal susceptibility in PD and is a feature of both familial and sporadic disease, as well as in toxin-induced Parkinsonism. Recently, the mechanisms by which PD-associated mitochondrial proteins phosphatase and tensin homolog deleted on chromosome 10 (PTEN)-induced putative kinase 1 (PINK1) and parkin function and induce neurodegeneration have been identified. In addition, increasing evidence implicates other PD-associated proteins such as α-synuclein (α-syn) and leucine-rich repeat kinase 2 (LRRK2) in mitochondrial dysfunction in genetic cases of PD with the potential for a large functional overlap with sporadic disease. This review highlights how recent advances in understanding familial PD-associated proteins have identified novel mechanisms and therapeutic strategies for addressing mitochondrial dysfunction in PD.
DOI: 10.1016/j.tibs.2015.02.003
PubMed: 25757399
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Ryan</name><affiliation wicri:level="4"><nlm:affiliation>Oxford Parkinson's Disease Centre, Department of Physiology, Anatomy and Genetics, Le Gros Clark Building, University of Oxford, South Parks Road, Oxford, OX1 3QX, UK.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Oxford Parkinson's Disease Centre, Department of Physiology, Anatomy and Genetics, Le Gros Clark Building, University of Oxford, South Parks Road, Oxford, OX1 3QX</wicri:regionArea><orgName type="university">Université d'Oxford</orgName><placeName><settlement type="city">Oxford</settlement><region type="nation">Angleterre</region><region type="région" nuts="1">Oxfordshire</region></placeName></affiliation></author><author><name sortKey="Hoek, Selim" sort="Hoek, Selim" uniqKey="Hoek S" first="Selim" last="Hoek">Selim Hoek</name><affiliation wicri:level="4"><nlm:affiliation>Oxford Parkinson's Disease Centre, Department of Physiology, Anatomy and Genetics, Le Gros Clark Building, University of Oxford, South Parks Road, Oxford, OX1 3QX, UK.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Oxford Parkinson's Disease Centre, Department of Physiology, Anatomy and Genetics, Le Gros Clark Building, University of Oxford, South Parks Road, Oxford, OX1 3QX</wicri:regionArea><orgName type="university">Université d'Oxford</orgName><placeName><settlement type="city">Oxford</settlement><region type="nation">Angleterre</region><region type="région" nuts="1">Oxfordshire</region></placeName></affiliation></author><author><name sortKey="Fon, Edward A" sort="Fon, Edward A" uniqKey="Fon E" first="Edward A" last="Fon">Edward A. Fon</name><affiliation wicri:level="4"><nlm:affiliation>McGill Parkinson Program, Department of Neurology and Neurosurgery, Montreal Neurological Institute and Hospital, McGill University, Montréal, Québec H3A 2B4, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>McGill Parkinson Program, Department of Neurology and Neurosurgery, Montreal Neurological Institute and Hospital, McGill University, Montréal, Québec H3A 2B4</wicri:regionArea><orgName type="university">Université McGill</orgName><placeName><settlement type="city">Montréal</settlement><region type="state">Québec</region></placeName></affiliation></author><author><name sortKey="Wade Martins, Richard" sort="Wade Martins, Richard" uniqKey="Wade Martins R" first="Richard" last="Wade-Martins">Richard Wade-Martins</name><affiliation wicri:level="4"><nlm:affiliation>Oxford Parkinson's Disease Centre, Department of Physiology, Anatomy and Genetics, Le Gros Clark Building, University of Oxford, South Parks Road, Oxford, OX1 3QX, UK. 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Mitochondrial dysfunction is increasingly appreciated as a key determinant of dopaminergic neuronal susceptibility in PD and is a feature of both familial and sporadic disease, as well as in toxin-induced Parkinsonism. Recently, the mechanisms by which PD-associated mitochondrial proteins phosphatase and tensin homolog deleted on chromosome 10 (PTEN)-induced putative kinase 1 (PINK1) and parkin function and induce neurodegeneration have been identified. In addition, increasing evidence implicates other PD-associated proteins such as α-synuclein (α-syn) and leucine-rich repeat kinase 2 (LRRK2) in mitochondrial dysfunction in genetic cases of PD with the potential for a large functional overlap with sporadic disease. This review highlights how recent advances in understanding familial PD-associated proteins have identified novel mechanisms and therapeutic strategies for addressing mitochondrial dysfunction in PD.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25757399</PMID><DateCreated><Year>2015</Year><Month>03</Month><Day>27</Day></DateCreated><DateCompleted><Year>2015</Year><Month>09</Month><Day>28</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>22</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0968-0004</ISSN><JournalIssue CitedMedium="Internet"><Volume>40</Volume><Issue>4</Issue><PubDate><Year>2015</Year><Month>Apr</Month></PubDate></JournalIssue><Title>Trends in biochemical sciences</Title><ISOAbbreviation>Trends Biochem. Sci.</ISOAbbreviation></Journal><ArticleTitle>Mitochondrial dysfunction and mitophagy in Parkinson's: from familial to sporadic disease.</ArticleTitle><Pagination><MedlinePgn>200-10</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.tibs.2015.02.003</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0968-0004(15)00022-5</ELocationID><Abstract><AbstractText>Parkinson's disease (PD) is a progressive neurodegenerative disorder characterised by the preferential loss of dopaminergic neurons in the substantia nigra. Mitochondrial dysfunction is increasingly appreciated as a key determinant of dopaminergic neuronal susceptibility in PD and is a feature of both familial and sporadic disease, as well as in toxin-induced Parkinsonism. Recently, the mechanisms by which PD-associated mitochondrial proteins phosphatase and tensin homolog deleted on chromosome 10 (PTEN)-induced putative kinase 1 (PINK1) and parkin function and induce neurodegeneration have been identified. In addition, increasing evidence implicates other PD-associated proteins such as α-synuclein (α-syn) and leucine-rich repeat kinase 2 (LRRK2) in mitochondrial dysfunction in genetic cases of PD with the potential for a large functional overlap with sporadic disease. This review highlights how recent advances in understanding familial PD-associated proteins have identified novel mechanisms and therapeutic strategies for addressing mitochondrial dysfunction in PD.</AbstractText><CopyrightInformation>Copyright © 2015 Elsevier Ltd. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ryan</LastName><ForeName>Brent J</ForeName><Initials>BJ</Initials><AffiliationInfo><Affiliation>Oxford Parkinson's Disease Centre, Department of Physiology, Anatomy and Genetics, Le Gros Clark Building, University of Oxford, South Parks Road, Oxford, OX1 3QX, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hoek</LastName><ForeName>Selim</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Oxford Parkinson's Disease Centre, Department of Physiology, Anatomy and Genetics, Le Gros Clark Building, University of Oxford, South Parks Road, Oxford, OX1 3QX, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fon</LastName><ForeName>Edward A</ForeName><Initials>EA</Initials><AffiliationInfo><Affiliation>McGill Parkinson Program, Department of Neurology and Neurosurgery, Montreal Neurological Institute and Hospital, McGill University, Montréal, Québec H3A 2B4, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wade-Martins</LastName><ForeName>Richard</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Oxford Parkinson's Disease Centre, Department of Physiology, Anatomy and Genetics, Le Gros Clark Building, University of Oxford, South Parks Road, Oxford, OX1 3QX, UK. Electronic address: richard.wade-martins@dpag.ox.ac.uk.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>J-0901</GrantID><Agency>Parkinson's UK</Agency><Country>United Kingdom</Country></Grant><Grant><Agency>Canadian Institutes of Health Research</Agency><Country>Canada</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>03</Month><Day>08</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Trends Biochem Sci</MedlineTA><NlmUniqueID>7610674</NlmUniqueID><ISSNLinking>0968-0004</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051844">alpha-Synuclein</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008928" MajorTopicYN="N">Mitochondria</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051844" MajorTopicYN="N">alpha-Synuclein</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Parkinson's disease</Keyword><Keyword MajorTopicYN="N">mitochondrial dysfunction</Keyword><Keyword MajorTopicYN="N">mitophagy</Keyword><Keyword MajorTopicYN="N">oxidative stress</Keyword><Keyword MajorTopicYN="N">α-synuclein</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2014</Year><Month>11</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2015</Year><Month>02</Month><Day>06</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2015</Year><Month>02</Month><Day>11</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2015</Year><Month>3</Month><Day>12</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2015</Year><Month>3</Month><Day>12</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2015</Year><Month>9</Month><Day>29</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">25757399</ArticleId><ArticleId IdType="pii">S0968-0004(15)00022-5</ArticleId><ArticleId IdType="doi">10.1016/j.tibs.2015.02.003</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Canada</li><li>Royaume-Uni</li></country><region><li>Angleterre</li><li>Oxfordshire</li><li>Québec</li></region><settlement><li>Montréal</li><li>Oxford</li></settlement><orgName><li>Université McGill</li><li>Université d'Oxford</li></orgName></list><tree><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Ryan, Brent J" sort="Ryan, Brent J" uniqKey="Ryan B" first="Brent J" last="Ryan">Brent J. Ryan</name></region><name sortKey="Hoek, Selim" sort="Hoek, Selim" uniqKey="Hoek S" first="Selim" last="Hoek">Selim Hoek</name><name sortKey="Wade Martins, Richard" sort="Wade Martins, Richard" uniqKey="Wade Martins R" first="Richard" last="Wade-Martins">Richard Wade-Martins</name></country><country name="Canada"><region name="Québec"><name sortKey="Fon, Edward A" sort="Fon, Edward A" uniqKey="Fon E" first="Edward A" last="Fon">Edward A. Fon</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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